Treating central nervous system diseases

ABSTRACT

A method of treating humans suffering from central nervous system diseases, such as Alzheimer&#39;s disease, Parkinsons&#39;s disease, senile dementia. The treatment consists of inducing into the patient&#39;s blood stream at least one from the group consisting of: sex hormones and anabolic hormones. Growth hormone is also be used in those patients in advanced stages of the disease, or in those patients where it has been determined that a low level of growth hormone is present. A method of diagnosing Alzheimer&#39;s disease, senile dementia, by the determination of the levels of the hormones somatotropin (human growth hormone) and somatomedin-C (IGF-I) after the administration of the Aroonsakul-Allen provocative test is also disclosed. Blood-sera samples are taken at certain time periods after the administration of L-Dopa, and the samples are tested for the levels of these hormones. These levels are then compared against the levels for normal subjects.

CROSS-REFERENCE TO RELATED APPLICATIONS

This is a continuation of co-pending application Ser. No. 156,242 filedon Feb. 16, 1988, which application is a continuation-in-part ofApplicant's co-pending application Ser. No. 666,254, filed Oct. 29,1984, now U.S. Pat. No. 4,791,099, which is a continuation-in-part ofSer. No. 852,645, filed Apr. 16, 1986 now U.S. Pat. No. 4,727,041.

BACKGROUND OF THE INVENTION

The present invention is directed to a method of treatment for centralnervous system diseases. These diseases for which the present inventivemethod has been found useful are: Alzheimer's disease; Parkinson'sdisease; senile dementia; essential tremor; senile tremor; andcerebellar atrophy and cerebral atrophy; multiple sclerosis;cerebrovascular accident. Each of these has been found to affectdifferent portions of the brain. Alzheimer's disease affects the portionof the brain vital to memory retention, the cortex. Parkinson's diseaseis known to affect the nerve cells of the basal ganglia. Cerebellaratrophy is known to affect the nerve cells of the cerebellum. It hasalso been determined that in each of the above diseases, intrinsicdepression develops, which is usually associated with an entirelydifferent portion of the brain than those affected by the above-nameddiseases. It is also known that in each of these diseases characterizedby biochemical lesions in enzymes, membranes, or structure proteins ofparticular components, cellular atrophy is the result, which is a slowprocess of cellular deterioration, sometimes deferred bes, but leadingto cellular atrophy, and eventually resulting in serious functionalloss, causing the symptoms associated with each of the diseases. Suchcellular atrophy generally occurs with advancing age, but, owing tothese diseases, the processes are somehow speeded up, in a manner notknown or understood at the present time. What is certain, however, isthat in any cellular breakdown, the enzymes required for proteinsynthesis are lacking. Further, it is also apparent that this lack ofenzyme formation, and concomitant lack of protein synthesis, are causedby some interruption in the neural network through which biochemicalsignals are generated and transported. Thus, the very problem of each ofthese diseases runs to the basic structure of life: To wit, RNA and DNA,ribo nucleic acid and deoxyribonucleic acid, which program each cell toprovide the necessary enzymes for life-sustaining activity.

Heretofore, there has been no effective method of treatment of each ofthe above-named diseases. In the case of Parkinson's disease, L-Dopa hasbeen employed and has achieved some success. However, the period ofefficacy of L-Dopa is limited to a few months. In the case ofAlzheimer's disease, and the remainder of the above-named diseases,ergoloid myselates have been used to some small success.

The present invention is also directed to a method of diagnosingAlzheimer's Disease in human beings. Presently-used techniques fordetermining Alzheimer's disease include neuropsychological testing whichcompares the mental status of the patient relative to a norm, as well asthe patient's cognitive dysfunction. Such testing also tests for mooddepressions, agitation, irritability, and the like, all of which aresymptoms of Alzheimer's disease. Other diagnostic tools and methods are:The use of a brain atlas beam test or EEG (electroencephalogram) whichdemonstrate increases in delta and theta waves. It is, of course, mostimportant that a correct diagnosis be determined in order to decide uponthe best treatment. The present invention is directed towards theincorporation of a novel diagnosis for Alzheimer's disease and seniledementia, that may be used in conjunction with other standard testingmethods, or may be used alone for such determination, since this noveldiagnosis has been found to be very accurate, especially when used inconjunction with conventional diagnostic tests for other chronicdegenerative diseases of the CNS form which similar indications mayresult. It has been known that the drug levodopa (L-Dopa), a common drugfor treating Parkinson's disease, causes increased secretion of thegrowth hormone somatotropin (HGH-human growth hormone). This finding ofAroonsakul and Allen provocative test (AA provocative test) such asL-Dopa's provocative stimulation of the pituitary gland to secrete HGHwas used as the basis for viewing the functioning of the peripheralnervous system (PNS) as an aminergic neuronetwork. Furthermore, sincethe hormone somatomedin-C (often referred to as IGF-I, for insulin-likegrowth factor) is directly dependent upon the secretion of HGH by thepituitary gland, there has been established a direct linkage betweenincreased secretion of HGH and increased production of the hormonesomatomedin-C, which is produced chiefly in the liver and kidneys. Theuse of L-Dopa to markedly increase the secretions of somatotropin and,consequently, the production of somatomedin-C in the human body has ledto what is generally termed the "L-Dopa provocative test". This test isused to determine the normal functioning of the anterior region of thepituitary gland responsible for the HGH production. Generally, the AAprovocative test is used by detecting the increase of HGH and IGF-I in ablood serum by the use of radioimmunoassay (RIA), which determines thepresence or absence or the amounts of a certain hormone in a serum bythe use of a radioactive agent, used in vitro. RIA involves separationof the labelled antigen that is of interest into bound-unbound fractionsafter the interaction with an antibody in the presence of the unknownquantity of unlabelled antigen to be measured. The radioactive elementused in this determination is usually I-125.

Somatotropin is a growth hormone (polypeptic-link amino acid incharacter), secreted by the anterior region of the pituitary gland. Thisis also known as the human growth hormone (HGH), and is the precursor ofthe hormone somatomedin-C (IGF-I), produced by the liver and kidneys.According to the present invention, it has been discovered that patientssuffering from Alzheimer's disease have a deficiency of somatotropinproduction which leads to a deficiency of somatomedin-C levels, and thatexogenous stimulation by a drug to cause increased secretions of HGH innormal human subjects, does not function normally in Alzheimer'spatients. Though it has been known to have increased levels of IGF-I inthe blood with reduced levels of HGH, these instances are rare and canbe taken into consideration when determining the diagnosis according tothe present invention.

SUMMARY OF THE INVENTION

The present invention consists of a method of treating patientssuffering from the above-named diseases with the hormones: sex hormonesand anabolic hormones. For male patients, androgens are used, orsuitable anabolic hormone substitutes are used. For female patientsestrogens are used in combination with androgens or anabolic hormones.Nonsteroidal anti-inflammatory drugs and vasodilaters may be used incombination with the hormone treatment to ensure that the blood deliversthe hormone or hormones to the brain. Further, the hormone method oftreatment may be supplemented with growth hormones alone or incombination, which are known for their anabolic tendencies, especiallyin those cases where there has been detected a noticeable loss of suchgrowth hormone in the patient's system, which growth hormones alsoexhibit remarkable rejuvenating properties.

It is a primary objective of the present invention to provide a noveldiagnostic technique and method by which positive identification ofAlzheimer's disease in a human being may be established definitively.

It is also an objective of the present invention to use any dopaminergicdrug, catecholamine, serotonin, amphetamine, causing immediate excesssecretion of the hormones HGH and IGF-I, as well as any drug creatingthe same excess secretion.

DESCRIPTION OF THE DRAWING

The invention will be more readily understood with reference to theaccompanying drawing, wherein:

FIG. 1 is a bar-chart showing the levels of the hormone somatotropin inblood sera at the end of specified periods obtained from the results ofthe L-Dopa AA provocative test;

FIG. 2 is a bar-chart similar to FIG. 1 for the hormone somatomedin-C;

FIG. 3 is graph showing the comparison between the human growth hormonelevels of a group of normal subjects as well as the graphs for thosediagnosed as suffering from Alzheimer's disease and senile dementia;

FIG. 4 is a graph showing the levels of brain neurotransmitter,acetylcholineesterase, present in blood samples according to the methodof diagnosing of the present invention.

DETAILED DESCRIPTION OF THE INVENTION

To reverse the degenerative nature of central nervous disorder disease,such as Parkinson's disease, Senile Dementia, Alzheimer's disease,senile tremor, and the like, and diseases especially associated withdementia, it has been discovered that treatment methods utilizing thesynthesizing, metabolic effects of androgens, estrogens, and anabolichormones have reversed the degenerative nature of the diseases, and haverestored patients suffering from the diseases to more normal andproductive lives, with the alleviation of many of the symptoms of thediseases. Further, upon continual and prolonged treatment with theabove-named group of hormones, there has not been found any diminutionof efficacy of the treatment, nor any serious contraindications andadverse side effects.

In one patient suffering from diagnosed Alzheimer's disease and earlystage Parkinson's disease, which patient was sixty years old and weighedone-hundred eighty pounds, he was given 10 mg. of fluoxymesterone USPdaily. In conjunction with the fluoxymesterone, the patient was given 1mg. of ergolid myselates four times a day; 50 mg. of dipyridamole, fourtimes a day; and acetyl salicylic acid enteric coated, four times a day,all taken orally. Within one week of the start of this treatment, thepatient experienced noticeable improvement, including the cessation ofParkinsonism tremor, and a wider span of attentiveness. In about onemonth from the start of the treatment, the patient stopped bed-wetting,and was able to concentrate on television, and othermentally-stimulating activities. Within about two months, the patient'sintellectual capacity increased so that he could carry on a conversationwith another person. Within about three months, the patient was able todress himself, and take a bath by himself. Within about four months, thepatient was able to smile, and laugh occasionally. Within about fivemonths, the patient was able to retain in his memory recent occurrencesand happenings. When the above-described treatment and medicine waseliminated, the patient regressed. After resumption of the treatmentwith fluoxymesterone, with the other drugs above-named, and in theirpreviously given doses, the patient again responded and started torecover from the degenerative nature of the diseases

In the treatment of central nervous system disorders, and especiallythose where dementia is present, it has been found that treatingpatients with the following hormones has caused alleviation of thedegenerative nature of the diseases, and has resulted in putting thepatient back on the road toward normalcy. These hormones belong to thegroup: Androgens for male patients; androgen-estrogen combination forfemale patients; anabolic hormones for either male or female patients;or a combination of any of the three classes within this group.

In the above-cited case history of one male patient who was treated withthe synthetic androgen and chorionic gonadotropin, any of the followingother androgens could have been used in lieu of, or in conjunction with,the fluoxymesterone; Testesterone; methyltesterone; and oxymethone.Furthermore, the patient could have been treated with any of thefollowing anabolic hormones in lieu of the androgen, or in combinationtherewith: Oxymetholone; oxandrolone; ethylestrenol; stanozolol;nandolone; phenpropionate; decanoate; and methandriol. Whereas in thecase of using the fluoxymesterone, a daily dosage of 10 mg. was providedthe patient, in the case of the use of other androgens, either singly orin combination with another androgen, the precise dose could vary.However, it has been found that a minimum dose of 1 mg. of any type ofandrogen above-named is preferred. Below such level, the beneficialresults above-noted would likely not occur.

Further, combinations of anabolic hormones alone, or anabolic hormoneswith androgens, may also be used to find the precisely-desired anaboliceffect to be had on the central nervous system of the patient, againwith the minimum daily dosage of 1 mg., either for combinations, orindividually-administered hormones.

Since a patient suffering from the diseases of the central nervoussystem, for which the treatment of the present invention has provensuccessful, also suffers from other ailments, either because thesediseases strike primarily those advanced in age or because of otherfactors, it has been found necessary to also treat the patient withother drugs in order to ensure that the hormone used is adequately andsafely delivered into the blood stream of the patient, and to the sitein the brain affected by the disease, so as to act on the degenerativenerve cells. Toward this end, as shown by the above-cited case, thepatient is typically treated also with vasodilater and non-steroidalanti-inflammatory drugs, to ensure that the hormone is delivered to thebrain. Further, ergoloid myselates are also used, the use of which fordementia has been known in the art. Among vasodilaters, any of thefollowing group may be used, either singly, or in combination:Dipyridamole; cyclospasmol; nylidinhydrochloride; papvarinehydrochloride; and isoxsuprine hydrochloride. Further, any well-knownvasodilater may be used, the above being given only by way of example.For non-steroidal anti-inflammatory drugs, any of the following may beused singly or in combination: Aspirin; ibuprofen, indomethacin;tolmetin sodium; and piroxicam. Also, any other well-known non-steroidalanti-inflammatory drug may be used, the above being given only by way ofexample.

Patients who are in the late and/or vegetative stages need othermedication in addition to the medication mentioned above. For women,estradiol, a major anabolic sex hormone in a female is needed. For men,androgen, a major anabolic sex hormone in a male is needed. Thus, in onecase history of a female patient 78 years of age, weighing approximatelyone-hundred fifty pounds, diagnosed as having Alzheimer's disease, thepatient was given the following, orally: 1.25 mg. conjugated estrogenonce a day; 10 mg. methyltetosterone once a day; 1 mg. ergoloid myselateUSP four times a day; 50 mg. dipyridamole four times a day; and 300 mg.acetyl salicylic acid enteric coated four times day.

The ergolid myselate helps, it is thought in the art, that it will serveto prevent the cell's temporary loss of protein; the dipyridamoleincrease cerebral blood flow; and the acetyl salicylic acid helps toprevent clots among other beneficial results. Just as in the case of themale patient noted above, this female patient experienced marked andfast rejuvenation, dissipation of dementia, increased mental alertness,and a general vitalization such that many of her Alzheimer diseasesymptoms by conventional diagnosis; but senile dementia disappeared bynew biochemical diagnosis in FIGS. 3 and 4.

Besides the use of conjugated estrogen, any estrogen from the followinggroup may be used singly or in combination: Estradiol; estrone; estriol.Further, gonadotropins and chorionic gonadotropins may also be used,singly or in combination. Also, another androgen or an anabolic hormonecould have been used successfully instead of the methyltestosterone.

In conjunction with the above-disclosed treatment, in these patientswhere it has been determined that the level of growth hormone in theirsystem is below normal for their size, sex, and age bracket, theabove-administering of drugs is supplemented with a growth hormone tore-establish normal levels thereof in the patients. These growthhormones, also of potent anabolic efficacy, serve to restore bodyfunction to a state receptive to treatment of the present invention inthose cases where growth hormone levels are deficient. Further, thegrowth hormone may also be used in those patients having normal levelsof old age thereof, if it has been found that treatment with theandrogen or anabolic hormones alone or in combination have notadequately provided success. Typically, if, after six months treatmentwith the present invention, improvement has not been shown,administering of growth hormones should be instituted, e.g. chorionicgonodotropin in combination. In the advanced stages of the diseases, agrowth hormone is also used alone at the outset of treatment, sinceowing to its increased and magnified positive metabolic effect, agreater and more concentrated inducement of nerve cell regeneration isneeded as described in the diagnostic method of senile dementiaAlzheimer style.

It is also indicated that the method of treatment as described in thepresent invention is successful for the alleviating of at least somesymptoms for most patients in the incipient, beginning or intermediatestages of the above-named diseases because of the following:

1. General increase in cerebral blood flow which enhances oxidation,including the normal metabolism of the brain cells;

2. Decrease of catabolism of protein and amino acids;

3. Enhancement of protein anabolism, leading to increased activity ofbrain cells, with the concomitant increase in red blood cell production;

4. Increase in the retention of calcium and sodium, which improve theaxon-presynapticpostsynaptic cell transmission;

5. Increase of intercellular protein, which increases the formation ofDNA andd RNA;

6. The revitalization of the nerve cell body dendrite and axons of thepre-synaptic and post-synaptic cells.

It is, of course, to be understood that the dosage given during the useof the treatment of the present invention is dependent upon the weight,size, age, and the like of the patient being treated. Further, any otherwell-known and equivalent sex hormone and anabolic hormone may be usedin addition to those listed above, as long as the anabolicmanifestations thereof are prevalent.

It has also been determined that, for female patients suffering from theabove-named central nervous system degenerative diseases, the use ofestradiol alone in suitable dosage provides sufficient anabolic effect,so that the use of an anabolic hormone supplemental to the female sexhormone is not needed. Estradiol has ample anabolic effect itself topreclude the need of the additional use of an androgen or anabolichormone. The same holds true for the female gonadotropic sex hormones.Since gonadotropic sex hormones offer potent anabolic effects as well,the use of an androgen and/or anabolic hormone is not needed. However,owing to the relative lack of anabolic effect of conjugated estrogensand estrones, then androgen and/or anabolic hormone would be required ina female patient, when treating her with either a conjugated estrogen orestrone sex hormone. In advanced stages of the above-named degenerativediseases, the use of a gonadotropic female sex hormone is desirable,either alone or in combination with a growth hormone or somatropinalone. The dosage, of course, will vary depending upon the age, size,and weight of the patient. The amount of initial dosage of gonadotropichormone and chorionic gonadotropic hormone preferably is that dosagepresently-used to treat men and women having low levels of sex anabolichormones. Since use of all of the above hormones causes increasedproduction of human growth hormone, the mechanism by which the method ofthe present invention is efficacious, human growth hormone should beused alone when the patient lacks the power to create HGH on his own.

In order to properly diagnose Alzheimer's disease, it has beendiscovered that patients suffering from this disease show a depletion ofthe human growth hormone somatotropin (HGH) and the HGH-dependenthormone somatomedin-C (IGH-I) which makes connective tissue, die on skinand joints. The growth hormone is secreted by the pituitary gland, whilesomatomedin-C is secreted mainly by the liver and kidneys by stimulationof somatotropin. This discovery of the lack of proper levels of thesetwo hormones, in combination with the fact that Alzheimer's patientslack the capabilities of producing these hormones endogenously even whenexogenous stimuli are created in the body of the patient, has led to themethod of diagnosis of the present invention. According to the presentinvention, the L-Dopa provocative test of Aroonsakul and Allen is usedto cause increased secretions of these two hormones, or somatropinalone, in order to determine if the pituitary gland, and the liver andkidneys, are capable of producing these hormones in response to thisprovocative test. It is important that not only the absolute levels ofthese two hormones in the peripheral blood serum be tested before theL-Dopa provocative test of Aroonsakul and Allen but also the levels ofthe increase, if any, produced by the L-Dopa provocative test, in orderto determine the current stimulation-capabilities of the peripheralnervous system and the hypothalamus, as well as the beta-adrenergic,alph adrenergic, and dopaminergic control systems. It is believed thatthe dominant control system is the dopaminergic, which is why L-Dopacauses increased secretions of HGH. For example clonidine propenolol,serotonin, ergoloid myselate causes andrenergic stimulation of the brainwhich will increase HGH.

The secretion of somatotropin by the pituitary gland is dependant uponmany factors, some of them being well-known, such as physical exercise,physical and hypoglycemic stresses, low-protein intake and others.Endogenous triggers of HGH release include sleep. Whether exogenous orendogenous, the changes in the secretion of the growth hormone(smatotropin) by the pituitary gland are directly dependent upon by thehormone "growth-hormone releasing-hormone" (GHRH) produced by thehypothalamus, which acts directly upon the pituitary gland in order tocause increase secretion of HGH. Exogenous injection of GHRH into theblood system will result in direct increased secretion of HGH. Thesecretion of HGH, in turn, causes the increased secretion ofsomatomedin-C by the liver and kidneys, which somatomedin-C is also usedas a feedback loop to the hypothalamus to regulate the secretion of GHRHand, thus, the secretion of HGH. The secretion of HGH is also inhibitedby the hormone somatostatin, a cyclic peptide having fourteen aminoacids, produced by the pancreas. Somatostatin also acts in a feedbackloop with the hypothalamus to inhibit production of GHRH and HGH.

It has been the discovery, according to the present invention thatpatients suffering from Alzheimer's disease lack proper and normallevels of HGH and somatomedin-C, and also lack the capabilities ofproducing increased amounts of these hormones in response to exogenousstimuli that tend to cause substantially large and immediate increasesof secretions in these two hormones, such as occurs during theAroonsokul-Allen provocative test (dopomine, catecholamine, serotonin).It is the method of the present invention to use the L-Dopa provocativetest to cause sudden and substantial increases in the secretions of thehormones HGH and somatomedin-C. By using radioimmunoassay techniques fordetecting the levels of these hormones in the blood serum at chosen timeintervals, the results thereof may be compared with the norm for the ageof the patient, to thereby guage if the pituitary gland is capable ofreacting to this stimuli to increase production of HGH, so that a firmdiagnosis of Alzheimer's disease may be made.

According to the method of the present invention for diagnosingAlzheimer's disease, one day prior to the use of the Aroonsokul-Allenprovocative test provocative test, a dosage of 8mg. og L-dopa perkilogram-of-weight of the patient is administered to the patient inorder to activate the HGH-secreting capabilities of the pituitary gland.On the next day, after an overnight fast, the L-dopa provocative test isgiven, with a dosage of 15 mg. of L-dopa per kilogram-of-weight of thepatient. A blood sample is taken just prior to the dosage of 8 mg. ofL-dopa per kg. on the day prior to the L-Dopa provocative test, andblood samples are also taken immediately before the start of the L-Dopaprovocative testing, and every 30 minutes after the dosage of 15 mg./kg.has been administered. Each blood serum is then tested by RIA techniquesto determine the absolute levels of somatotropin and somatomedin-C, andcompared against the normal values for the age of the patient beingtested. Referring to FIG. 1, there is shown a bar-chart comparing thelevels of somatotropin and somatomedin-C obtained by RA techniques forthe five blood sera taken during the provocative test with the levelsfor normal subjects aged fifty and over. The shaded bars representtypical levels of a patient who has Alzheimer's disease, while theunshaded bars indicate the levels for a normal person aged fifty andover, for the five sera assayed. As it may be seen, for normal subjects,the readings at times: 0 minutes, 30 minutes, 60 minutes, 90 minutes,and 120 minutes are, approximately: 2.00 ng/ml; 3.75 ng/ml; 7.90 ng/ml;6.05 ng/ml; and 4.45 ng/ml. For patients suffering from Alzheimer'sdisease the corresponding values are, approximately: 0.02 ng/ml; between0.03 ng/ml and 1.85 ng/ml; 2.15 ng/ml; 2.05 ng/ml; and 1.85 ng/ml. Thevalues indicated for the normal subjects are the statistical meanaverage. The highest value shown in FIG. 1, for a patient suffering fromAlzheimer's disease, for each of the sera tested by RIA is that lyingoutside of the standard statistical error associated with the RIAtesting.

FIG. 2 shows similar results for the RIA of the hormone somatomedin-C.For normal subjects age 50 and over, the values from RIA of this hormoneare approximately: 1.95 ng/ml; 4.00 ng/ml; 8.05 ng/ml; 5.90 ng/ml; and4.45 mg/ml. The corresponding values of Alzheimer's disease patients,are approximately: 0.10 ng/ml; 1.65 ng/ml; 2.15 ng/ml; 2.00 ng/ml; and2.05 ng/ml.

It is, of course, possible to use different time periods in which theblood sera are taken for subsequent RIA analysis, with these resultsbeing compared to a standard for subjects aged 50 and over for the sametime periods tested. According to the present invention, substantialdifferences in levels of these two hormones during the AA provocativetest as compared with the normal subjects is a positive and definitiveindication of Alzheimer's disease. Furthermore, the absolute differencesbetween the tested sera and the levels for normal subjects may also beused for an indication as to the state of advancement of Alzheimer'sdisease in the patient. Tested levels far outside the statistical normadjusted for standard statistical error would mean a more advanced stageof the disease.

There will be some instances where the levels of somatotropin willincrease and be similar to those of normal subjects, but the levels ofsomatomedin-C will fall far short of those for normal subjects, as couldoccur if the patient were suffering from liver disease. Thus, the AAprovocative test would show a mixed result. In this case, furthertesting would be required, and a positive determination of Alzheimer'sdisease would have to be confirmed in conjunction with other,currently-used, prior art methods of diagnosis, such as EEG testing,neuropsychological testing, and the like. Also, where the results fromthe AA provocate test do not show enough differences between the patientbeing tested and the norm, such as might occur if the values determinedby RIA were not outside the statistical mean error of the normal group,then these other conventional methods of diagnosis would be used inconjunction with the method of the present invention. Whereas, both HGHand IGF-I deficiency in children may occur, as in dwarfism, such matcheddeficiency in adults is not known to indicate any other disease but thatdiscovered according to the present invention. Since during basal,morning conditions there usually cannot be detected any differencesbetween normal subjects and those with HGH deficiency, the provocativetest is required, as described above.

Any other HGH-provocative agent may be used instead of L-Dopa. Forexample, bromocriptine, propanolol, serotonin, catecholamine clonidine,other dopaminergic stimuli, and glucagon, a small peptide that mediatesthe flow of glucose to insulin-independent tissues. Of course, the timeperiods between which the blood sera are taken will depend upon thesomatotropin-provocative agent used. Other constraints and conditionswill, of course, change dependent upon the HGH-provocative used, andwill be obvious to one having ordinary skill in the art. For example,for glucagon as the HGH-provocative, overnight fasting would not berequired.

The same type of provocative test above described may also be used fordiagnosing senile dementia in human beings, as shown in FIGS. 3 and 4,which are graphs of the levels of the hormone being detected for thesubject patient diagnosed as suffering from Alzheimer's disease orsenile dementia as compared to a controlled group thereof. The samemethod of diagnosing is carried out as above described when using thedesired provocative test. It has also been discovered that the detectionof the proportion of the brain neurotransmitter, acetylcholineesterase ,is also indicative of a diagnosis of Alzheimer's disease or seniledementia, as shown in the graphs of FIG. 4 where the ordinate is timeand the abcissa is the proportion of the brain neuro-transmitter,acetylcholineesterase, to the total blood sample for normal subjects andthose suffering from Alzheimer's disease or senile dementia. In FIG. 4,the graph labelled 1 shows the readings of the proportion of the baintransmitter acetlycholineestrase for normal subjects, while the graphlabelled 2 shows the upward limit of the readings for the proportion ofthe brain transmitter indicative of Senile Dementia. The graph labelled4 indicates the readings at or below which is an indication ofAlzheimer's Disease. The region between the graphs labelled 3 and 4 is atransition region, readings lying therein not being clearly definitiveas to Senile Dementia or Alzheimer's Disease.

The method of treating a patient diagnosed as suffering from Alzheimer'sdisease or senile dementia via the above-described provocative test andmethod of diagnosing is determined by the results of that diagnosticmethod and the calculated deficiency of somatropin in the blood of thepatient. The range of somatropin dosages is between 0.015 mg to 0.8 mg.per kilogram of body weight of the patient. Such somatropin replacementmay take the form of actual dosages of somatropin, or human growthhormone, (synthetic somatropin may be used) in the case of advancedstages and where the depletion is marked, or may take the form ofdosages of testosterone, estradiol, and the other anabolic hormonesabove-enumerated, which themselves indirectly cause the production ofsomatropin in the body, to thereby efficaciously treat the disease asabove-described in the case of less-advanced stages.

It has also been discovered that dosages of somatropin is effective intreating the following: Chronic degenerative disease of the joints, suchas arthritis; hypoplastic anemia in aging; osteoporosis during aging;atrophy of the visceral organs such as the kidneys, liver, spleen duringaging; atrophy of muscle tissue during aging. Furthermore, it has beendiscovered (that dosages of somatropin, within the range above-defined,is effective in treating general weakness, lack of energy, slowmovement, and is even effective in smoothing out wrinkles andeliminating wrinkles altogether in some circumstances.

While specific embodiments of the invention have been shown anddescribed, it is to be understood that numerous changes andmodifications thereof may be made without departing from the scope,intent and spirit of the invention as set forth in the appended claims.

What I claim is:
 1. A method for treating central nervous systemdiseases in human beings said diseases selected from Sensile DementiaParkinson's disease, cerebral atrophy, Alzheimer's disease, cerebellaratrophy, senile tremor, and essential tremor, comprising:including intothe blood stream of the human being suffering from the disease aneffective dose of at least one of a gonadatropin and chorionicgonadotropin.
 2. The method according to claim 1, further comprisinginducing into the bloodstream effective dosage from a group consistingof: androgens, anabolic hormones, and androgen-anabolic hormonecombinations.
 3. The method according to claim 2, further comprisinginducing into the bloodstream of a female patient effective dosage ofhuman growth hormone.
 4. The method according to claim 1, furthercomprising inducing into the bloodstream of a female patient effectivedosage of human growth hormone.
 5. The method according to claim 2,wherein said androgens is taken from a group consisting of:testosterone, methyltestosterone, fluoxymesterone, and oxymethone.